The article discusses the two main classes of lung cancer: non–small-cell lung cancer (NSCLC), mainly the lung adenocarcinoma (LUAD) subtype originating from alveolar type 2 (AT2) cells, and small cell lung cancer (SCLC), where pulmonary neuroendocrine cells (PNECs) are the primary cell of origin. SCLC carries the worst prognosis, causing over 200,000 deaths annually worldwide. Approximately 10% of patients with LUAD driven by mutated epidermal growth factor receptor (EGFR) and undergoing EGFR targeted therapy develop resistance to treatment through histological transformation (HT) into SCLC. Similar transformations to neuroendocrine tumors are occasionally observed in patients with prostate adenocarcinoma undergoing androgen deprivation therapy. However, the mechanisms behind these HTs and the involved transition stages have remained elusive. Gardner et al. identified the sequential stages LUAD cells undergo during HT to SCLC in mice, shedding light on this challenging conversion in human cancer.
cellular respiration
chloroplast
prophase
cytokinesis
cell cycle
telophase
centromere
malignant neoplasm
what are cell cycle regulators
what is cancer?
what are cell cycle regulators?
what type of transport is used to move oxygen out of the lungs?
cell metabolism
what is the monomer of hemoglobin?
what is a benign tumor
what happens if the apc gene is mutated
how do mutated tumor suppressor genes affect the cell cycle
what are oncogenes
in some types of colon cancer, stem cells have a mutation in the apc gene. what happens if the apc gene is mutated?
to cause cancer proto-oncogenes require
normally, tumor suppressor genes inhibit the cell cycle. how do mutated tumor suppressor genes affect the cell cycle?
adenocarcinoma of the lung
inhibitory proteins are encoded by
small cell carcinoma lung cancer
normally, proto-oncogenes stimulate the cell cycle. what are oncogenes and how do they affect the cell cycle?